1 Association Between Left Ventricular Global Longitudinal Strain and Adverse Left Ventricular Dilatation After ST-segment Elevation Myocardial Infarction Joyce et al: GLS and LV Dilatation after STEMI Emer Joyce 1 , MB BCh BAO, MRCPI; Georgette E. Hoogslag 1 , MSc; Darryl P. Leong 1,2 , MBBS, PhD; Philippe Debonnaire 1 , MD; Spyridon Katsanos 1 , MD; Helèn Boden 1 , MD; Martin J. Schalij 1 , MD, PhD; Nina Ajmone Marsan 1 , MD, PhD; Jeroen J. Bax 1 , MD, PhD; Victoria Delgado 1 , MD, PhD 1 Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands; 2 Discipline of Medicine, University of Adelaide and Flinders University, Adelaide, Australia. Correspondence: Victoria Delgado, MD, PhD Dept. of Cardiology, Leiden University Medical Center Albinusdreef 2, 2333 ZA Leiden, the Netherlands Phone: +31 71 526 2020, Fax: +31 71 526 6809 Email address: [email protected]DOI: 10.1161/CIRCIMAGING.113.000982 Journal Subject Codes: [31] Echocardiography; [4] Acute myocardial infarction; [115] Remodeling Cardiology, Leiden University Medical Center, Leiden, the Neth edicine, University of Adelaide and Flinders University, Adelaid e o L id U i it M di l C t Card d d d dio o io io olo lo lo o ogy g g g g , , , Le L L L L iden University Me Me Me Me Medi d d d d cal Center, Le L L L L iden, the Neth e e e e edi di di i dicine, Un niv v ver r rs s sity y y y o o o of Ad A A A A el el laide de e a an n nd F F F F Fli li li li lind nd nd n n ers s s Un Un niv v v v ve e ersity y y y, , Ad A el l la ai a d e: o, MD MD, Ph Ph Ph Ph PhD D D D L L L i i id d d U U U i i i i i it t M M M d d di i i l l l C C C t t by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from by guest on June 10, 2018 http://circimaging.ahajournals.org/ Downloaded from
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1
Association Between Left Ventricular Global Longitudinal Strain and
Adverse Left Ventricular Dilatation After ST-segment Elevation
Myocardial Infarction
Joyce et al: GLS and LV Dilatation after STEMI
Emer Joyce1, MB BCh BAO, MRCPI; Georgette E. Hoogslag1, MSc;
Darryl P. Leong1,2, MBBS, PhD; Philippe Debonnaire1, MD;
Spyridon Katsanos1, MD; Helèn Boden1, MD; Martin J. Schalij1, MD, PhD;
Nina Ajmone Marsan1, MD, PhD; Jeroen J. Bax1, MD, PhD;
Victoria Delgado1, MD, PhD
1Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands;
2Discipline of Medicine, University of Adelaide and Flinders University, Adelaide, Australia.
Correspondence: Victoria Delgado, MD, PhD Dept. of Cardiology, Leiden University Medical Center Albinusdreef 2, 2333 ZA Leiden, the Netherlands Phone: +31 71 526 2020, Fax: +31 71 526 6809 Email address: [email protected]
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retrospective analysis of clinically acquired data, the Institutional Review Board waived the
need of patient written informed consent.
2D transthoracic echocardiography
Patients were imaged in the left lateral decubitus position using a commercially available
system (Vivid 7, GE Healthcare, Horten, Norway) equipped with a 3.5-MHz transducer.
Analysis of echocardiographic images was performed offline using EchoPAC version 11.0.0
software (GE Healthcare). LV end-systolic volume (LVESV), LVEDV and LVEF were
quantified at baseline and at 3 and 6-months follow-up using the Simpson’s biplane
technique.14 The intra- and interobserver agreement for assessment of LVEDV at our
laboratory has been previously reported as 93% and 92% respectively.15 Qualitative
assessment of regional wall motion was performed for each patient by dividing the LV into
16 segments. Each segment was then scored individually based on its motion and systolic
thickening (1=normokinesis, 2=hypokinesis, 3=akinesis, 4=dyskinesis) and WMSI was
calculated as the sum of the segment scores divided by the number of segments scored.14
Severity of mitral regurgitation (MR) was graded according to current recommendations.16
Diastolic function was assessed according to standard recommendations.17 Left atrial volume
was evaluated with the biplane Simpson’s technique and indexed to body surface area
(LAVI).14
Global longitudinal strain analysis
LVGLS was quantified from the apical 4-, 2- and 3-chamber views stored as digital cine-
loops and processed offline using commercially available speckle-tracking analysis software
(EchoPac 112.0.1, GE Medical Systems, Horten, Norway). Images were recorded with frame
rates >40 frames per second to ensure reliable analysis by the software. The end-systolic
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gional wall motion was performed for each patient by dividing h
ch segment was then scored individually based on its motion a d
ormokinesis, 2=hypokinesis, 3=akinesis, 4=dyskinesis) and WM
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frame was defined in the apical long-axis view by marking the closure of the aortic valve.
Following this, the LV endocardial border was traced at end systole in all 3 apical views and
the automatically created region of interest was manually adjusted to the thickness of the
myocardium. Tracking quality was assessed in all segments and if tracking was of poor
quality segments were discarded. LVGLS was provided by the software as the average value
of the peak systolic longitudinal strain of the 3 apical views, using a 17-segment model, in a
bull’s-eye plot (Figure 1). As previously reported, the intra- and interobserver variability for
the measurement of LVGLS in our institution is 0.1±2.2% and 0.2±0.8% respectively.18
Statistical analysis
Continuous, normally distributed variables are presented as mean and standard deviation
(SD) or standard error (SE) as appropriate. Non-normally distributed data are presented as
median and interquartile range. Categorical variables are presented as frequencies and
percentages. The total population was divided into 2 groups based on the median value of
LVGLS. Continuous variables were compared between the 2 groups using Student-t test,
Mann Whitney U test or X2 test as appropriate.
The primary modeling approach was linear mixed effects model analysis with LVEDV as the
dependent variable and time (0, 3- and 6-month) as the principal fixed effect. The main
predictor variable of interest was baseline LVGLS. Of note, missing data points did not
exclude subjects from the analysis, as inherent in the mixed modeling analysis structure. To
determine whether baseline LVGLS was associated with subsequent change in LVEDV, it
was modelled in an interaction term with time. If this group-time interaction term was
significant, it indicated a time-dependent relationship between baseline GLS and LVEDV.
Post hoc testing was then performed to determine the time points at which LVEDV differed
between the LVGLS groups. Other important and potentially confounding baseline clinical
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quartile range. Categorical variables are presented as frequencie
total population was divided into 2 groups based on the median
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LVEF in predicting 30-day infarct size.23 In our large population of contemporary STEMI
patients treated with primary PCI, a post-revascularization LVGLS value >-15.0% was
significantly associated with clinical characteristics traditionally indicative of larger infarct
size (diabetes, multivessel disease, higher biomarker levels). Additionally, these patients had
significantly more impaired global and regional systolic and diastolic function parameters
(including LVEF, WMSI and E’) as compared to the group of patients with more preserved
myocardial shortening (LVGLS -15.0%).
LVGLS and LV remodeling
Despite the demonstrated role of LVGLS in accurately identifying the extent of global
myocardial injury and dysfunction after infarction, few studies in the contemporary era have
specifically related LVGLS measurement in the acute phase after STEMI to the risk of LV
remodeling at follow-up. A substudy of the VALIANT (valsartan in acute myocardial
infarction trial) study including 603 post-STEMI patients with LV dysfunction, demonstrated
no significant association between myocardial longitudinal strain rate and LV remodeling.26
However, those patients were enrolled prior to the systematic use of primary PCI and other
current guideline-based anti-remodeling therapies. Studies involving modern era STEMI
patients, which have demonstrated an association between LVGLS and LV remodeling, are
limited by small numbers, variable LV remodeling definitions and shorter follow-up
periods.27, 28 The current evaluation considerably expands on previous studies by relating
baseline LVGLS measurement in a large cohort of contemporary STEMI patients to accepted
echocardiographic outcomes on systematic 3- and 6-month follow-up. Patients with LVGLS
>-15% were significantly more likely to display pathological LV dilatation at both 3- and 6-
months after STEMI. This relationship remained significant even after adjusting for multiple
clinical parameters known to influence post-STEMI outcome. Importantly, repeating the
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ed LVGLS measurement in the acute phase after STEMI to the r
llow-up. A substudy of the VALIANT (valsartan in acute myo a
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analysis per quartile of GLS (supplemental file) showed a stepwise relationship between less
negative (more impaired) GLS and progressive LV dilatation, with the greatest and most
significant increase in LVEDV at both 3- and 6-month occurring in those patients in the
highest quartile of GLS (>-12.1%). The finding that LVGLS measurement prior to discharge
can identify patients at increased risk of LV dilatation is particularly relevant given it can be
quantified at rest and without need for pharmacological stressors, expensive contrast media or
exposure to ionizing radiation.
LVGLS versus WMSI in risk stratification after STEMI
Previous studies have consistently shown that WMSI evaluation is superior to LVEF for early
risk assessment after STEMI.6, 29 WMSI and LVGLS were recently shown to accurately
identify substantial infarction in non-STEMI patients prior to revascularization.30 However,
segmental motion and thus WMSI, unlike LVGLS, may be influenced by tethering of scar
tissue by adjacent viable myocardium. In the current study, we confirmed an advantage of
LVGLS over WMSI for early risk stratification after STEMI. While baseline WMSI was
independently associated with LV remodeling at 3- and 6-month follow-up, the addition of
LVGLS to a model containing WMSI provided incremental value for prediction of LVEDV
increase. Although the absolute differences in LVEDV at follow-up appear small, LVGLS
was both incremental to WMSI and significantly reclassified additional patients over and
above traditional post-STEMI risk parameters. Given these findings and the fact that LVGLS
provides a semi-automated, quantitative measure of LV systolic function its future use for
risk stratification in all STEMI patients is highly foreseeable.
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This was a retrospective evaluation. However, it reports prospectively collected real-world
data on a large cohort of modern era STEMI patients treated optimally according to a
dedicated, guideline-based protocol.11 Patients in cardiogenic shock requiring supportive
therapy were not included in this study; therefore these findings may not apply to this
important patient group. However, these patients represent a high-risk group and additional
strategies for risk stratification are less clinically relevant. Additionally, echocardiography
was performed within 48 hours after STEMI in all patients; the dynamic nature of LV
function recovery following STEMI may lead to an underestimation of the systolic function
during this time period. However, in the final adjusted model, time from reperfusion to
baseline echocardiography did not have a significant effect on the relationship between
baseline LVGLS and follow-up LV dilatation.2, 6 2D Simpson’s biplane method to assess
LVEDV may be less accurate in the presence of foreshortening or irregular LV geometry and
is associated with a high variability.31 However, the prognostic value of LVEDV using this
method of assessment has been proven 32 and it remains the currently recommended method
to assess LV systolic function on 2D echocardiography.14 Changes in heart rate during
follow-up and their association with LV dilatation were not assessed. However, the aim of
the current study was to assess the effect of LVGLS measured in the acute phase after
STEMI on follow-up LV dilatation as compared to other baseline characteristics (including
discharge heart rate) known to influence later risk of remodeling. Additionally, changes in
medication at follow-up were not systematically recorded. However, it is known from a
systematic overview of angiotensin converter enzyme inhibition in STEMI patients that most
of the survival benefit is observed in the first week.33, 34 Intra- and interobserver variability
measurements were not performed as part of the current study protocol. However, our
laboratory performs LVGLS measurements in a standardized manner. The reproducibility
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up. This large contemporary registry study confirms the benefit
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1. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990;81:1161-72. 2. St John SM, Pfeffer MA, Plappert T, Rouleau JL, Moye LA, Dagenais GR, Lamas GA, Klein M, Sussex B, Goldman S, . Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril. Circulation. 1994;89:68-75. 3. White HD, Norris RM, Brown MA, Brandt PW, Whitlock RM, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation. 1987;76:44-51. 4. Byrne RA, Ndrepepa G, Braun S, Tiroch K, Mehilli J, Schulz S, Schomig A, Kastrati A. Peak cardiac troponin-T level, scintigraphic myocardial infarct size and one-year prognosis in patients undergoing primary percutaneous coronary intervention for acute myocardial infarction. Am J Cardiol. 2010;106:1212-7. 5. Chia S, Senatore F, Raffel OC, Lee H, Wackers FJ, Jang IK. Utility of cardiac biomarkers in predicting infarct size, left ventricular function, and clinical outcome after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. JACC Cardiovasc Interv. 2008;1:415-23. 6. Moller JE, Hillis GS, Oh JK, Reeder GS, Gersh BJ, Pellikka PA. Wall motion score index and ejection fraction for risk stratification after acute myocardial infarction. Am Heart J. 2006;151:419-25. 7. Antoni ML, Mollema SA, Delgado V, Atary JZ, Borleffs CJ, Boersma E, Holman ER, van der Wall EE, Schalij MJ, Bax JJ. Prognostic importance of strain and strain rate after acute myocardial infarction. Eur Heart J. 2010;31:1640-7. 8. Mollema SA, Delgado V, Bertini M, Antoni ML, Boersma E, Holman ER, Stokkel MP, van der Wall EE, Schalij MJ, Bax JJ. Viability assessment with global left ventricular longitudinal strain predicts recovery of left ventricular function after acute myocardial infarction. Circ Cardiovasc Imaging. 2010;3:15-23. 9. Sjoli B, Orn S, Grenne B, Vartdal T, Smiseth OA, Edvardsen T, Brunvand H. Comparison of left ventricular ejection fraction and left ventricular global strain as determinants of infarct size in patients with acute myocardial infarction. J Am Soc Echocardiogr. 2009;22:1232-8. 10. Vartdal T, Brunvand H, Pettersen E, Smith HJ, Lyseggen E, Helle-Valle T, Skulstad H, Ihlen H, Edvardsen T. Early prediction of infarct size by strain Doppler echocardiography after coronary reperfusion. J Am Coll Cardiol. 2007;49:1715-21. 11. Antoni ML, Boden H, Delgado V, Boersma E, Fox K, Schalij MJ, Bax JJ. Relationship between discharge heart rate and mortality in patients after acute myocardial infarction treated with primary percutaneous coronary intervention. Eur Heart J. 2012;33:96-102. 12. O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Jr., Chung MK, de Lemos JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zhao DX, Anderson JL, Jacobs AK, Halperin JL, Albert NM, Brindis RG, Creager MA, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Kushner FG, Ohman EM, Stevenson WG, Yancy CW. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362-e425.
2ML, Mollema SA, Delgado V, Atary JZ, Borleffs CJ, Boersma E,E, Schalij MJ, Bax JJ. Prognostic importance of strain and s rlSA, De ado V, Bertini M, Antoni ML, Boersma E, Holm n
all EE, Schalij MJ, Bax JJ. Viabili assessment with lobal eain predicts recovery of left ventricular function after acutet
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